三株登革2型病毒广东分离株结构蛋白E基因序列测定及分析

目的对广东省分离的3株登革2型病毒(DEN2)的结构蛋白E基因扩增、克隆、测定及分析,了解流行株之间的相互关系及基因型.方法应用RT-PCR技术扩增广东省不同年份流行的3株DEN2型病毒的结构蛋白E基因.分别克隆到PMD18 T载体,转化JM109宿主菌,挑取阳性克隆进行鉴定及序列测定.结果3株DEN2病毒结构蛋白E基因序列长度均为1 485 bp,编码495个氨基酸.其核苷酸(氨基酸)的同源性分别是GD06/93与GD19/2001为98%(98%)、GD06/93与GD08/98为92%(95%)、GD08/98与GD19/2001为91%(94%).3株DEN2与国际参考株比较表明GD06/93与澳大利亚TSV01株共享序列非常接近,核苷酸(氨基酸)的同源性为99%(99%);GD19/2001和澳大利亚TSV01株核苷酸(氨基酸)的同源性为98%(98%);GD08/98与泰国株ThNH-P28/93核苷酸(氨基酸)同源性为98%(98%).结论GD06/93、GD19/2001与TSV01亲缘关系较近,属同一基因型.GD08/98与TnNH-P28/93共享序列非常接近,属同一基因型.     

广东省流行的3株登革热2型病毒基因组全序列测定及分析

目的测定广东省3株登革热2型病毒的全序列,探讨其来源及基因型。方法运用RT PCR法扩增来自广东省的登革热2型GD09/93、GD05/98和GD19/2001病毒株的全序列,采用遗传距离法构建进化树。结果3株登革热2型病毒的全基因组长度均为10 723 nt,5′及3′端各有一非编码区,结构基因和非结构基因位于基因组97~10 269 nt之间,共编码3391个氨基酸,读码结构完全相同。GD05/98与GD09/93、GD05/98与GD19/2001、GD09/93与GD19/2001之间的碱基序列同源性分别为93.3%、92.4%和97.6%,氨基酸序列同源性分别为96.7%、96.5%和98.5%。结论3株登革热2型病毒均对乳鼠致病,与对乳鼠不致病的参考株（DEN2-04株）比较共有18个氨基酸位点的差异引起极性或电荷变化,PrM-134、NS2A-153、NS4B-102所带电荷的变化对抗原性影响较大。GD05/98株与泰国分离株同为Ⅱ基因型,GD09/93和GD19/2001株与印度尼西亚、澳大利亚、台湾株分在Ⅳ基因型;表明我国登革热2型病毒有不同的基因型,而不同时期也存在同一种基因型传播。     

浙江省2002年2例柯萨奇B5病毒VP1区基因特性分析

目的：研究2002年浙江省病毒性脑膜脑炎病原CoxB5病毒VP1区的基因特征。方法：用Hep-2和RD两种细胞对患者脑脊液和粪便标本进行病毒分离，提取病毒RNA，再用RT—PCR扩增病毒VP1区基因片断，对纯化产物进行核苷酸序列测定，采用DNAMAN和Bioedit软件进行分析处理。结果：两株CoxB5病毒的VP1区核苷酸长度均为849bp，二者核苷酸同源性为98.7％，氨基酸同源性达100％。结论：浙江省两株CoxB5病毒为同一性状毒株，它们的亲缘关系与侵犯中枢神经系统的CoxB5的原型株AF—114383CoxB5(Swend—16—1998)最为接近。但这两株CoxB5毒株与欧美国家相比，核苷酸同源性仅为79.3％～81．5％，氨基酸同源性为96.82～97．53％，核苷酸序列有了18.5％～20.7％的变异，与国外报道的CoxB5株之间存在一定的差异。这两株病毒与安徽明光市2001年从无菌性脑膜脑炎病人粪便中分离到的两株CoxB5病毒MG—18—2001和MG—39—2001在同一小分枝上，核苷酸同源性达98．5％～98．9％，氨基酸同源性达99．29％～99.65％。     

宁波市麻疹病毒血凝素基因的序列分析

目的：探讨现阶段在宁波市流行的麻疹野病毒的基因型别和特征。方法：在2004年和2005年医院住院麻疹病人中采集含漱液分离麻疹病毒，获得8株麻疹野病毒。通过RT-PCR方法扩增其中两株麻疹病毒血凝素（H）基凼全序列并对其进行序列测定和分析。比较这两株麻疹病毒和Genbank中麻疹病毒的各基因型代表株的同源性。结果：两株宁波麻疹毒株ningbo04-2和ningbo05-2的H基因之间核苷酸同源性为97．7％，与川基因型代表株China93-7之间核苷酸同源性分别为98．3％，97．7％。与它们在核苷酸水平上同源性最高的毒株分别是zhejiang05-2，china94-7，其同源性分别达到99，7％，99．4％。ningbo04-2在氨基酸240位由丝氨酸（S）突变成天冬酰胺（N），造成一个潜在的N型糖基化位点丢失。结论：宁波市麻疹流行株属于H1型，至少存在H1a，HIb两组。     

广东省麻疹病毒血凝素基因的序列分析

目的 探讨广东省麻疹病毒的基因型别和特征。方法 对2000年和2001年分别在广东省中山和韶关地区分离的两株麻疹病毒，通过RT－PCR方法扩增麻疹病毒血凝素（H）基因全序列，并克隆pMD18-T Vector进行序列测定；并分析这两株麻疹病毒和Genbank中麻疹病毒的各基因型代表株序列的同源性。结果 两株广东麻疹流行株H基因之间同源性为97％，和它们在核苷酸水平上同源性最高的毒株分别是China93-4和China94-7，达到99％。和其它已知麻疹病毒的21个基因代表株相比，广东省麻疹毒株在核苷酸水平上最大变异为7．0％，其中广东省2000年流行株在氨基酸240位由丝氨酸（S）突变成天门酰胺（N），造成一个N型糖基化位点丢失。结论 广东省麻疹流行株属于H1基因型。     

霍乱弧菌主要毒力和管家基因序列分析

目的分析广东霍乱弧菌（VC）代表菌株主要毒力基因和管家基因序列。方法PCR扩增霍乱弧菌的主要毒力基因（ctxAB和tcpA）和管家基因（dnaE、hlyA、mdh和recA）、基因测序、对序列进行生物信息学分析。结果不同年代分离的2株埃尔托型（EVC）产毒株和1株0139群VC产毒株的主要毒力基因序列与国内外相关报告比较，ctxA基因及推测的氨基酸序列的同源性分别为99．7％～100％和98．8％～100％．ctxB基因及推测的氨基酸序列的同源性分别为98．8％～100％和96．8％～100％，tcpA基因序列与EVC国际标准株N16961 100％同源。3株产毒株的dnaE、hlyA、mdh和recA基因序列同源性分别为99．8％～100％，100％，99．5％～99．8％和100％，氨基酸序列同源性分别为100％．100％，98．5％～99．3％和100％；3株产毒株和O139群VC非产毒株的管家基因序列同源性分别为97．0％～97．2％，91．8％，94．1％～94．4％，96．9％，氨基酸序列同源性分别为100％，94．6％，94．3％～98．5％和99．7％。结论广东省不同年代EVC产毒株和O139群VC产毒株的群体遗传学关系高度密切，而与O139群VC非产毒株较远，O139群VC产毒株可能起源于EVC产毒株。     

庚型肝炎病毒杭州株E2／NS1基因区的克隆及序列分析

目的 获得散发性庚型肝炎病毒杭州株E2／NS1区部分核酸序列。方法 选择1例浙江杭州散发性庚型肝炎患,从其血清中分离HGVRNA,通过逆转录套式聚合酶链反应（RT－nPCR)法,扩增该散发性HGV（HZ－2株）E2／NS1区部分cDNA片段,然后克隆到质粒pGEX-4T-3中,并进行核苷酸序列分析。结果 HGV杭州株与河北株（HGVC964、美国株）（HGU44402）的核苷酸同源性为92．5％和89．8％,氨基酸同源性为98．0％和93．9％。结论 该项研究将为HGV诊断试剂盒的研制及基因工程疫苗的研制提供资料。     

2010一2011年湖南省郴州市手足口病EV71型VP1区基因序列分析

目的了解2010-2011年湖南省郴州市手足口病EV71病毒的基因特征,为手足口病的预防控制提供科学依据。方法从2010-2011年郴州市各县（市、区）送检的手足口病肛拭子标本中随机挑选60份标本采用RD细胞进行病毒分离,采用Realtime—RT—PCR方法检测肠道病毒核酸,挑选14株致细胞病变阳性且EV71核酸检测阳性的标本（其中2010年的4株均为郴州市手足口流行夏季高峰期分离株,2011年的毒株主要为冬季高峰期分离株）,采用RT—PCR法扩增出EV71分离株的VP1区片段,随后进行VP1区核苷酸序列测定和分析,并使用生物信息学方法作基因特性分析。结果郴州市14株EV71毒株在生物进化树上与CAa亚型的代表株属同一分支。14株EV71毒株之间核苷酸序列的同源性在96．1％～100．0％之间,氨基酸序列的同源性在99．3％～100．0％之间;与A、B、C各基因型和亚型代表株EV71VP1编码区核苷酸和氨基酸序列同源性分析表明,郴州各分离株与安徽阜阳2008年毒株C4a亚型代表株（EU703812）的同源性最高,其中核苷酸同源性在91．8％-93．3％之间,氨基酸同源性均为99．3％。14株分离株与安徽阜阳2008年毒株（C4a亚型代表株）VP1区段的氨基酸编码序列进行比较,发现K98E、S283T和A293S3处位点变异,重症病例与普通病例的EV71病毒VPI氨基酸变异无明显差异。结论2010-2011年郴州市手足口病的优势毒株EV71属于C4a基因亚型。郴州市各县（市、区）的EV71亲缘关系近,毒株基因较稳定,未发现氨基酸突变位点与病例类型有关联。     

福建省龙岩市2011年病毒性脑炎病例埃可病毒30型分析

目的分析龙岩市2011年病毒性脑炎病例埃可病毒[人肠道致细胞病变孤儿病毒,Enteric Cytopathogenic Human Orphan(ECHO)Virus]30型(ECHO30型)特征。方法对龙岩市2011年某医院病毒性脑炎住院病例采集脑脊液(Cerebrospinal Fluid,CSF)进行病毒分离、血清中和试验定型;选取4株ECHO30型分离株,测定VP1编码区序列,与国内外其他病毒株进行比较。结果从142份患者CSF标本中分离到ECHO30型20株、ECHO11型7株、ECHO6型10株。4株ECHO30型VP1编码区序列长度为606个核苷酸,编码202个氨基酸。4株的核苷酸和氨基酸同源性分别为97%~100%和88%~100%。与2000年Bastianni原型株的核苷酸和氨基酸同源性分别为81%~82%和81%~93%。与2010年山东省、2011和2012年福州市流行毒株核苷酸和氨基酸同源性分别为96%~100%和87%~100%。系统进化树分析显示,4株龙岩分离株同属基因型(Genotype)Ⅱ。结论龙岩市2011年病毒性脑炎病例的ECHO_(30)型为GenotypeⅡ。     

中国2006年麻疹野病毒血溶素基因特征分析

目的研究中国2006年流行的麻疹野病毒代表株血溶素蛋白（Fusion Protein,F）基因的分子特征,与其他年份毒株相比分析F基因的变异规律。方法从2006年各省（自治区、直辖市）送检的麻疹野病毒中选取9株代表株,使用逆转录-聚合酶链反应扩增病毒的F基因全长,并进行核苷酸序列测定,同时与中国疫苗株及其他年份毒株进行序列比对及基因亲缘性关系分析。结果2006年9株中国流行麻疹野病毒代表株,其核苷酸同源性为98．5％-99．8％,氨基酸同源性为99％-100％;与中国疫苗株沪。相比,其核苷酸同源性为95．4％-96．2％,氨基酸同源性为96．7％～97．2％;与1999～2003年代表株相比,其核苷酸同源性为97．9％-99．7％,氨基酸同源性为98．1％-100％。F基因3个糖基化位点（第32、64、70位氨基酸）、对病毒整合功能起着重要作用的第112位精氨酸（Arg）、第195位亮氨酸（Leu）未发生改变。结论中国2006年流行的麻疹病毒F基因变异不大,与其他年份毒株相比变异也不明显。F蛋白的重要功能位点未发生变异,F蛋白的变异与2006年麻疹流行无相关性。但由于F蛋白对病毒感染细胞和促使机体产生抗体具有重要意义,对F蛋白变异规律进行常规监测,对了解麻疹病毒变异规律和评价疫苗的保护效果具有重要意义。     

Novel agmatine and agmatine-like peptidomimetic inhibitors of the West Nile virus NS2B/NS3 serine protease

This communication reports the synthesis and inhibitory activities of novel non-covalent peptidomimetic inhibitors of the West Nile virus NS2B/NS3 protease containing a decarboxylated P1 arginine (agmatine; 4-aminobutylguanidine) and related analogues. One agmatine peptidomimetic (4-phenyl-phenacetyl-Lys-Lys-agmatine; compound 2) was shown to be a competitive inhibitor with a binding affinity of K_i 2.05 ± 0.13 μM and was inactive against thrombin (IC₅₀ > 100 μM). Our results suggest that peptidomimetics with agmatine at the P1 position could potentially be employed as starting tools in the design of non-covalent competitive protease inhibitors due to their relative stability and ease of chemical synthesis compared to inhibitors containing reactive electrophilic warheads.     

VP2-serotyped live-attenuated bluetongue virus without NS3/NS3a expression provides serotype-specific protection and enables DIVA

Bluetongue virus (BTV) causes Bluetongue in ruminants and is transmitted by Culicoides biting midges. Vaccination is the most effective measure to control vector borne diseases; however, there are 26 known BTV serotypes showing little cross protection. The BTV serotype is mainly determined by genome segment 2 encoding the VP2 protein. Currently, inactivated and live-attenuated Bluetongue vaccines are available for a limited number of serotypes, but each of these have their specific disadvantages, including the inability to differentiate infected from vaccinated animals (DIVA).BTV non-structural proteins NS3 and NS3a are not essential for virus replication in vitro, but are important for cytopathogenic effect in mammalian cells and for virus release from insect cells in vitro. Recently, we have shown that virulent BTV8 without NS3/NS3a is non-virulent and viremia in sheep is strongly reduced, whereas local in vivo replication leads to seroconversion. Live-attenuated BTV6 without NS3/NS3a expression protected sheep against BTV challenge. Altogether, NS3/NS3a knockout BTV6 is a promising vaccine candidate and has been named Disabled Infectious Single Animal (DISA) vaccine.Here, we show serotype-specific protection in sheep by DISA vaccine in which only genome segment 2 of serotype 8 was exchanged. Similarly, DISA vaccines against other serotypes could be developed, by exchange of only segment 2, and could therefore safely be combined in multi-serotype cocktail vaccines with respect to reassortment between vaccine viruses.Additionally, NS3 antibody responses are raised after natural BTV infection and NS3-based ELISAs are therefore appropriate tools for DIVA testing accompanying the DISA vaccine. To enable DIVA, we developed an experimental NS3 ELISA. Indeed, vaccinated sheep remained negative for NS3 antibodies, whereas seroconversion for NS3 antibodies was associated with viremia after heterologous BTV challenge.     

HCV NS3解旋酶基因原核表达载体pGEX-4T-1的构建

[目的]构建丙型肝炎病毒(HCV)非结构蛋白NS3解旋酶基因原核表达载体,为进一步研究和解析NS3的解旋酶基因对病毒复制的机制准备条件.[方法]将含有NS3基因的pMD-24/HCV NS3质粒转化感受态菌DH-5α并扩增;提取pMD-24/HCV NS3质粒;从pMD-24/HCV NS3质粒中扩增出NS3解旋酶基因;并将其插入到克隆载体pMD-18T中,再与表达载体pGEX-4T-1重组,以得到重组的原核表达载体pGEX-4T-1/NS3解旋酶.[结果]从pMD-24/HCV NS3质粒中扩增出的NS3解旋酶基因片断大小正确,经测序证明其碱基序列为编码目的基因的正确序列:电泳结果证明已将此片段克隆到pGEX-4T-1内.[结论]成功地构建了HCV NS3解旋酶基因的原核表达载体DGEX-4T-1/NS3解旋酶.     

甲型流感病毒H1N1亚型NS1蛋白真核表达载体的构建与表达

[目的]构建甲型流感病毒H1N1亚型NS1蛋白真核表达载体,并在293T细胞中表达.[方法]采用RT-PCR技术,从甲型流感病毒H1N1毒株提取的病毒总RNA中,扩增NS1全长基因,将其克隆至pMD18-T Vector中构建pMD18-T-NS1质粒,双酶切pMD18-T-NS1与PXJ40-HA后,构建真核表达载体PXJ40-HA-NS1,经酶切及测序鉴定后将质粒转染到293T细胞中,通过免疫印迹法鉴定NS1蛋白的表达.[结果]酶切、测序证明重组真核表达载体PXJ40-HA-NS1构建成功,免疫印迹法可见NS1基因编码蛋白表达.[结论]成功构建甲型流感病毒H1N1亚型NS1蛋白真核表达载体PXJ40-HA-NS1,并在293T细胞中传染表达,该表达载体的构建为后期建立稳定表达NS1蛋白的细胞模型和NS1蛋白功能研究提供了材料.     

Nanodelivery system enhances the immunogenicity of dengue-2 nonstructural protein 1, DENV-2 NS1

Nonstructural protein 1 (NS1) of dengue virus (DENV) is currently recognized as a dengue vaccine candidate. Unfortunately, most of non-replicating immunogens typically stimulate unsatisfactory immune responses, thus, the additional adjuvant is required. In this study, C-terminal truncated DENV-2 NS1 loaded in N,N,N, trimethyl chitosan nanoparticles (NS1_1-279TMC NPs) was prepared through the ionic gelation method. The immunogenicity of NS1_1-279TMC NPs was investigated using human ex vivo as well as the murine model. Through a human ex vivo model, it was demonstrated in this study that not only can TMC particles effectively deliver NS1_1-279 protein into monocyte-derived dendritic cells (MoDCs), but also potently stimulate those cells, resulting in increased expression of maturation marker (CD83), costimulating molecules (CD80, CD86 and HLA-DR) and markedly secreted various types of innate immune cytokines/chemokines. Moreover, mice administered with NS1_1-279TMC NPs strongly elicited both antibody and T cell responses, produced higher levels of IgG, IgG1, IgG2a and potently activated CD8⁺ T cells, as compared to mice administered with soluble NS1_1-279. Importantly, we further demonstrated that anti-NS1_1-279 antibody induced by this platform of NS1_1-279 effectively eliminated DENV-2 infected cells through antibody dependent complement-mediated cytotoxicity. Significantly, anti-DENV2 NS1_1-279 antibody exerted cross-antiviral activity against DENV-1 and −4 but not against DENV-3 infected cells. These findings demonstrate that TMC exerts a desirable adjuvant for enhancing delivery and antigenicity of NS1 based dengue vaccine.     

DNA vaccine against the non-structural 1 protein (NS1) of dengue 2 virus

Dengue is one of the most important mosquito-borne viral disease causing dengue fever and/or dengue shock syndrome/haemorrhagic fever. In some reports, the non-structural protein 1 (NS1) has been identified as a promising antigen for the development of vaccines against dengue virus (DENV). Apparently, it can elicit a protective antibody response with complement-fixing activities. In order to investigate the potential of a DNA vaccine based on the NS1 protein against DENV, we used the plasmid pcTPANS1, which contains the secretory signal sequence derived from human tissue plasminogen activator (t-PA) fused to the full length of the DENV-2 NS1 gene. All Balb/c mice intramuscularly inoculated with the pcTPANS1 presented high levels of NS1-specifc antibodies. Vaccinated animals were challenged with intracerebral DENV-2 virus inoculations and a 100% survival was observed. In general, results demonstrate that the pcTPANS1 plasmid is able to induce protection in mice, and then may be used as a vaccination approach against DENV in further assays.     

Heterogeneous genomic locations within NS3, NS4A and NS4B identified for genotyping and subtyping of Hepatitis C virus: A simple genome analysis approach

Hepatitis C virus (HCV) displays excessive genetic heterogeneity and exists in several genotypes and subtypes. Characterizing these genotypes and subtypes becomes extremely important for diagnostic and epidemiological reasons. Present study analyzed HCV genome using a simple genome analysis approach. We combined manual sectioning of a reference genome alignment (RA) followed by a comprehensive comparative phylogenetic analysis. The main aim was to identify heterogeneous locations on HCV genome suitable for genotyping/subtyping. HCV reference dataset, comprising of whole genome sequences from all HCV genotypes and subtypes, was aligned into an RA. The RA was manually clipped into overlapping sections of 500 bases, each 50 bases apart. Phylogeny for each section and RA was estimated using neighbor-joining phylogenetic method. Clustering pattern between section phylogenies and RA phylogeny was compared for similarity. Sections (locations on genome) with clustering similar to whole genome were selected since it displays comparable genetic heterogeneity making these sections suitable for genotyping/subtyping. Based on this conception, we identified new genomic locations on NS3, NS4A and NS4B suitable for genotyping and subtyping. Exact genomic positions for known genotyping locations, core and NS5B were also identified. Furthermore, phylogenetic analyses at such small genomic scale provided opportunities to explore evolutionary relationships usually overlooked.     

合并感染HIV对1b型HCV E2/NS1包膜区基因影响

目的 研究人类免疫缺陷病毒(HIV)感染对1b型丙型肝炎病毒(HCV) E2/NS1包膜区基因变异的影响,探讨2组间E2/NS1区基因序列同源性差异,为HCV/HIV合并感染者中HCV的治疗提供依据.方法 对河南省某有偿献血村进行随访,将得到的所有HCV阳性病例255例根据合并HIV感染的情况分成2组,并对其基因分型,然后进行逆转录( RT)-巢式PCR扩增1b型HCV E2/NS1包膜区基因,继而进行单链构象多态性分析(SSCP)、纯化后测序.结果 HCV单纯感染组和HIV/HCV合并感染组SSCP平均条带数分别为(3.4±0.55)、(2.6±0.55)条,差异有统计学意义(t =2.32,P =0.049);HCV单纯感染组和HIV/HCV合并感染组HCV E2/NS1包膜区同源性分别为76.7％和87.6％,差异有统计学意义(x2=20.13,P＜0.001);2组第一高变区(HVR-1)同源性分别为59.3％和81.9％,差异有统计学意义(x2=10.39,P=0.001);2组第3高变区(HVR-3)同源性分别为71.7％和83.9％,差异有统计学意义(x2=4.60,P=0.03);单纯HCV组中变异性较高的氨基酸位点在HCV/HIV合并感染组中表现出较高的保守性.结论 HIV感染对1b型HCV E2/NS1包膜区基因变异具有抑制作用,且其主要体现在HVR-1和HVR-3区.     

Genotyping atypical porcine pestivirus using NS5a

Atypical porcine pestivirus (APPV) is an emerging virus discovered in 2014 and it can cause congenital tremors in pigs. Molecular epidemiology serves as an essential tool in monitoring and controlling the disease. Virus epidemiology mainly relies on genome sequencing and phylogenetic characterization. Previous molecular epidemiology studies have been using different genes/regions for phylogeny, namely whole genome, Npro, and E2 coding sequences. However, with increasing number of APPV sequences available in GenBank, no systemic studies have been performed for detailed classification of APPV strains around the globe. The goal of this study is to propose a classification strategy or taxonomy of APPV strains at genotype, subgenotype, and isolate levels. A total of 76 whole genomes and 16 partial polyprotein coding sequences were analyzed for genetic variability and suitability of all individual genes for viral phylogenies. Our results revealed that, among all the viral genes, NS5a coding sequences were proved to be the most suitable alternative for tracing APPV strains supported by its capability of reproducing the same phylogenetic and evolutionary information as the whole viral genome did. Also, a reliable cutoff to accurately classify APPV at different levels is established. We propose a genotyping scheme with three well-defined genotypes (1–3) and 7 subgenotypes for genotype 1 (1.1–1.7). For whole genome analysis, a threshold value of 84%–91% pairwise identity allows separation of all APPV subgenotypes, whereas 80% identity clearly segregate the three major APPV genotypes. For NS5a gene analysis, 82%–91% identity allows subgenotype separation and 76% identity segregate APPV genotypes. Additionally, genetic distance of whole genome exhibits ≤8% in isolate level, 9%–14% in subgenotype level, and 17%–22% in genotype level, while for NS5a encoding sequences the genetic distance displays ≤9% in isolate level, 9.9%–19.1% in subgenotype level, and 21.6%–29.7% in genotype level. These allow a clear segregation among APPV genotypes, subgenotypes, and isolates. Therefore, the proposed strategy in this study provides a solid and improved basis for molecular phylogenetics to understand APPV genetic diversity, trace the origins and control the spread of new disease outbreaks.     

乙型流感病毒NSl基因的进化

NS1蛋白是由流感病毒第8个RNA片段(丙型流感病毒NS1由第7个片段)编码的RNA结合蛋白[1].研究表明,NS1蛋白与流感病毒宿主存在复杂的相互作用[2-5],是流感病毒主要的毒力因子[6].乙型流感病毒是导致流感暴发的主要病原之一,目前为止只发现一个亚型,宿主特异性较强[7].探讨乙型流感病毒NS1蛋白的变异规律,分析其起源和进化过程,对于监控流感病毒感染人群毒力的变化,预测流感病毒流行趋势以及流感减毒活疫苗株的筛选具有重要的参考意义.